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. 2018 Dec 17;9:5340. doi: 10.1038/s41467-018-07758-x

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — Reduced cytokine mRNA stability in IRE1α-deficient iNKT cells. a Splenic NKT1, 2 and 17 cells were isolated from control (n = 4) and CD4^cre;IRE1α^Δ/Δ (n = 4) mice, expanded and restimulated with anti-CD3/CD28 for 3 h prior to addition of actinomycin D. mRNA decay rates were determined by linear regression analysis. Data represent three independent experiments pooled. b−d Bulk splenic wild-type iNKT cells were expanded in vitro, restimulated with anti-CD3/CD28 for 3 h in the presence of APY29 and B-109, and then treated with actinomycin D. mRNA decay rates were determined as above. Data represent two independent experiments pooled. e Purified bulk splenic iNKT cells from control (n = 6) and CD4^cre;IRE1α^Δ/Δ (n = 6) mice were restimulated ex vivo with α-CD3/CD28 for 3 h, prior to addition of actinomycin D. Data represent two independent experiments pooled. Error bars show the mean ± s.e.m. p < 0.05 determined by linear regression analysis and ANOVA, n.d. not detected